Abstract
Cardiac arrhythmias are responsible for many cardiovascular disease-related deaths worldwide. While arrhythmia pathogenesis is complex, there is increasing evidence for metabolic causes. Obesity, diabetes, and chronically consuming high-fat foods significantly increase the likelihood of developing arrhythmias. Although these correlations are well established, mechanistic explanations connecting a high-fat diet (HFD) to arrhythmogenesis are incomplete, although oxidative stress appears to be critical. This review investigates the metabolic changes that occur in obesity and after HFD. Potential therapies to prevent or treat arrhythmias are discussed, including antioxidants.
Highlights
Cardiovascular disease (CVD), including coronary heart disease, heart failure, stroke, and hypertension, persists as the leading cause of death worldwide despite advances in medical treatment [1,2,3,4]
Public health concerns regarding the surge in obesity over the past few decades, concerning trends in dietary patterns, and the increased prevalence of CVD and arrhythmias motivate a closer examination of the metabolic impacts of a chronic high-fat diet (HFD), both concurrent with and independent of comorbidities such as obesity
This work showed that HFD suppressed mitophagy, and deletion of acetyl-CoA carboxylase 2 (ACC2)—which inhibits mitochondrial import of fatty acids—improved mitophagy and prevented cellular hypertrophy and a decrease in ejection fraction, which was seen in control mice after 24 weeks of high-fat diet-induced obesity [63]
Summary
Cardiovascular disease (CVD), including coronary heart disease, heart failure, stroke, and hypertension, persists as the leading cause of death worldwide despite advances in medical treatment [1,2,3,4]. In the U.S.A., elevated rates of CVD are caused by an increasing prevalence of risk factors including obesity, diabetes, and the consumption of foods high in fat and/or sugar [4,5,6,7]. Public health concerns regarding the surge in obesity (defined in humans as having a body mass index, or BMI, of 30.0kg/m2 or more) over the past few decades, concerning trends in dietary patterns, and the increased prevalence of CVD and arrhythmias motivate a closer examination of the metabolic impacts of a chronic high-fat diet (HFD), both concurrent with and independent of comorbidities such as obesity. The aim of this review is to examine the potential mechanisms that mediate the relationship between obesity or the long-term consumption of high-fat foods and the development of pro-arrhythmogenic metabolic conditions, as well as novel antioxidant approaches to pharmacological treatment. For a more clinically oriented review, the interested reader is referred to this recent publication: [9]
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